2. Membrane Transporter/Ion Channel Neuronal Signaling Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Autophagy
  3. Calcium Channel Reactive Oxygen Species (ROS) Autophagy
  4. Didrovaltrate

Didrovaltrate  (Synonyms: Didrovaltratum)

Cat. No.: HY-N3741 Purity: 92.0%
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Didrovaltrate (Didrovaltratum) is an L-type calcium channel blocker, ROS scavenger, autophagy enhancer, and lipid accumulation inhibitor. Didrovaltrate blocks L-type calcium currents in a concentration-dependent manner, shifts the current-voltage curve upward, modulates steady-state inactivation kinetics, and inhibits the nuclear translocation of glucocorticoid receptors. Didrovaltrate reduces ROS levels, downregulates the expression of muscle atrophy-related genes, enhances autophagy via lipophagy, and decreases Oleic acid-induced lipid accumulation. Didrovaltrate exhibits cytotoxic activity against cancer cells. Didrovaltrate can be used in research related to skeletal muscle atrophy, non-alcoholic fatty liver disease, breast cancer, lung cancer, gastric cancer, and prostate cancer.

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Didrovaltrate

Didrovaltrate Chemical Structure

CAS No. : 18296-45-2

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Didrovaltrate Related Antibodies

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N-type calcium channel L-type calcium channel P/Q-type calcium channel T-type calcium channel Calcium Channel

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Description

Didrovaltrate (Didrovaltratum) is an L-type calcium channel blocker, ROS scavenger, autophagy enhancer, and lipid accumulation inhibitor. Didrovaltrate blocks L-type calcium currents in a concentration-dependent manner, shifts the current-voltage curve upward, modulates steady-state inactivation kinetics, and inhibits the nuclear translocation of glucocorticoid receptors. Didrovaltrate reduces ROS levels, downregulates the expression of muscle atrophy-related genes, enhances autophagy via lipophagy, and decreases Oleic acid-induced lipid accumulation. Didrovaltrate exhibits cytotoxic activity against cancer cells. Didrovaltrate can be used in research related to skeletal muscle atrophy, non-alcoholic fatty liver disease, breast cancer, lung cancer, gastric cancer, and prostate cancer[1][2][3][4].

Cellular Effect
Cell Line Type Value Description References
A549 IC50
> 10 μM
Compound: 20
Cytotoxicity against human A549 cells after 24 hrs by MTT assay
Cytotoxicity against human A549 cells after 24 hrs by MTT assay
[PMID: 19245261]
Bel-7402 IC50
7.5 μM
Compound: 20
Cytotoxicity against human Bel7402 cells after 24 hrs by MTT assay
Cytotoxicity against human Bel7402 cells after 24 hrs by MTT assay
[PMID: 19245261]
HCT-8 IC50
6.6 μM
Compound: 20
Cytotoxicity against human HCT8 cells after 24 hrs by MTT assay
Cytotoxicity against human HCT8 cells after 24 hrs by MTT assay
[PMID: 19245261]
PC-3M IC50
3.8 μM
Compound: 20
Cytotoxicity against human PC3M cells after 24 hrs by MTT assay
Cytotoxicity against human PC3M cells after 24 hrs by MTT assay
[PMID: 19245261]
In Vitro

Didrovaltrate (30-100 μg/L) reduces the peak L-type calcium current (maximum L-type calcium current), decreasing it from 6.01 pA/pF to 3.45 pA/pF and 2.16 pA/pF, with inhibition rates of 42.6% and 64.1%, respectively[1].
Didrovaltrate (2.5-5 μM; 24 h) significantly downregulates the expression of muscle atrophy marker genes *Atrogin-1*, *Murf1* and *Mstn* in atrophic C2C12 myotubes induced by Dexamethasone (DEX) (HY-14648), restores the fusion index and myotube diameter, reverses C2C12 myotube atrophy, reduces ROS production, and inhibits the nuclear translocation of glucocorticoid receptor and FOXO3a[2].
Didrovaltrate (2.5-25 μM; 24 h) reduces the viability of Huh7 hepatocytes at concentrations of 10 μM and higher[3].
Didrovaltrate (10 μM; 24 h) reduces oleic acid (HY-N1446)-induced lipid accumulation in Huh7 hepatocytes in an Atg5-dependent manner[3].
Didrovaltrate (10 μM; 0-24 h) enhances autophagic flux in Huh7 hepatocytes and increases the formation of LC3 puncta in cells[3].
Didrovaltrate (1-100 μM; 48 h) potently inhibits the viability of MCF7 human breast adenocarcinoma cells, with an IC50 of 3.9 μM; after 48 h of treatment, this compound exhibits moderate to weak cytotoxic activity against the A549, HGC27, PC3, and HUVEC cell lines[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Didrovaltrate Related Antibodies

Real Time qPCR[2]

Cell Line: DEX-induced atrophic C2C12 myotubes
Concentration: 2.5, 5 μM
Incubation Time: 24 h (co-incubated with 5 μM DEX)
Result: Significantly downregulated the DEX-induced upregulation of Atrogin-1, Murf1, and Mstn mRNA expression.
Reduced Atrogin-1 expression to ~1.3-fold and ~1.4-fold of the untreated control (from a DEX-induced ~2.2-fold).
Reduced Murf1 expression to ~0.7-fold and ~0.6-fold of the untreated control (from a DEX-induced ~1.9-fold).
Reduced Mstn expression to ~1-fold and ~0.5-fold of the untreated control (from a DEX-induced ~4.5-fold).

Immunofluorescence[2]

Cell Line: DEX-induced atrophic C2C12 myotubes
Concentration: 2.5, 5 μM
Incubation Time: 24 h (co-incubated with 5 μM DEX)
Result: Restored the fusion index from DEX-induced ~42% of the untreated control to ~55% and ~56% respectively.
Restored mean myotube diameter from DEX-induced ~10 μm (from untreated control ~12 μm) to ~11 μm and ~12 μm respectively.
Shifted the myotube diameter distribution away from small diameters (<10 μm) toward larger diameters (>14 μm), reversing the DEX-induced shift toward smaller myotubes.

Western Blot Analysis[2]

Cell Line: DEX-induced atrophic C2C12 myotubes
Concentration: 2.5, 5 μM
Incubation Time: 24 h (co-incubated with 5 μM DEX)
Result: Reduced DEX-induced nuclear GR levels from ~2.81-fold of the untreated control to ~1.98-fold and ~1.81-fold of the untreated control respectively.
Reduced DEX-induced nuclear FOXO3a levels from ~3.75-fold of the untreated control to ~1.74-fold and ~1.53-fold of the untreated control respectively, effectively inhibiting DEX-induced nuclear translocation of both proteins.

Cell Viability Assay[3]

Cell Line: Huh7 hepatocytes
Concentration: 2.5, 5, 10, 25 μM
Incubation Time: 24 h
Result: Reduced cell viability to ~75% of control at 10 μM.
Reduced cell viability to ~38% of control at 25 μM.
Caused no significant changes in cell viability at 2.5 and 5 μM.

Western Blot Analysis[3]

Cell Line: Huh7 hepatocytes
Concentration: 10 μM; 10 μM (with 25 nM BafA1 for final 1 h)
Incubation Time: 0-24 h; 24 h (with 1 h BafA1 treatment)
Result: Increased LC3-II levels relative to LC3-I over time, with the highest ratio (1.5) observed at 24 hours.
Further increased LC3-II levels (ratio of 1.7) compared to BafA1 alone in the presence of BafA1.

Immunofluorescence[3]

Cell Line: Huh7 hepatocytes
Concentration: 10 μM
Incubation Time: 24 h
Result: Increased the formation of LC3 puncta compared to vehicle-treated cells.

Cell Cytotoxicity Assay[4]

Cell Line: human lung adenocarcinoma (A549), human breast adenocarcinoma (MCF7), human gastric carcinoma (HGC27), human prostate adenocarcinoma (PC3), human umbilical vein endothelial (HUVEC)
Concentration: 1-100 μM
Incubation Time: 48 h
Result: Inhibited cell viability of A549 cell line with an IC50 of 26.7 μM.
Inhibited cell viability of MCF7 cell line with an IC50 of 3.9 μM.
Inhibited cell viability of HGC27 cell line with an IC50 of 12.6 μM.
Inhibited cell viability of PC3 cell line with an IC50 of 69.3 μM.
Inhibited cell viability of HUVEC cell line with an IC50 of 14.8 μM.
Exhibited the most potent activity against the MCF7 breast cancer cell line.
Molecular Weight

424.48

Formula

C22H32O8
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

CC(O[C@@H]1[C@]2(CO2)[C@]([C@@H]3OC(CC(C)C)=O)([H])[C@](C(COC(CC(C)C)=O)=CO3)([H])C1)=O
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Purity & Documentation
References
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Didrovaltrate Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Didrovaltrate18296-45-2DidrovaltratumCalcium ChannelReactive Oxygen Species (ROS)AutophagyCa2+ channelsCa channelsC2C12 myotubesC2C12 myoblast cellsreactive oxygen speciesglucocorticoid receptorL-type calcium channelA549MCF7 human breast adenocarcinoma cellHuh7 hepatocytesHGC27autophagyInhibitorinhibitorinhibit

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